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. Author manuscript; available in PMC: 2019 Feb 27.
Published in final edited form as: Nat Genet. 2018 Aug 27;50(9):1271–1281. doi: 10.1038/s41588-018-0200-2

Fig. 1. Clinical cohort consolidation, response stratification, and mutational load investigation.

Fig. 1

(a) Data quality control for 249 samples included in final analysis. (b) Comparison of three published response metrics for determining OR vs. NR. (c) Comparison of tumor mutational burden between CR/PR vs. PD (For ‘All mutations’, p=0.0005 for CR/PR vs PD, p=0.0054 for CR/PR vs SD, and p=0.434 for SD vs PD; for ‘Nonsynonymous mutations’, p=0.0003 for CR/PR vs PD, p=0.0063 for CR/PR vs SD, and p=0.3769 for SD vs PD; for ‘Clonal nonsynonymous mutations’, p=0.00005 for CR/PR vs PD, p=0.011 for CR/PR vs SD, and p=0.151 for SD vs PD). Outlying points from patients with mutations/Mb > 101 are not shown (2 CR/PR, 1 SD, 3 PD). (d) Intratumoral heterogeneity across response groups (n=249 biologically independent samples, p=0.001 for CR/PR vs. PD, p=0.5122 for CR/PR vs SD). (e) Clinical response to immune checkpoint therapy broken down by intratumoral heterogeneity. For (c, d), p-values calculated by two-sided Mann-Whitney U *p<0.05, **p<0.005, ns = not significant. Boxplots show the median, first and third quartiles, whiskers extend to 1.5 × the interquartile range, and outlying points are plotted individually.